1550: Ecmo Rescue in Lamotrigine-Induced Cardiac Arrest in an Adolescent

Introduction: The diagnosis of pediatric ingestions is challenging due to often incomplete history and inability of readily available toxicology screens to detect most pharmaceuticals. We describe a severe toxidrome of an initially undetermined substance. Description: A 15-year-old female with ADHD and depression treated with viloxazine was transferred from an ED with slurred speech and ataxia. Initial blood work and non-contrasted CT head were unremarkable. An EKG showed sinus rhythm with normal intervals. On presentation, she had dilated pupils, dry mucous membranes, and erratic myoclonic jerks. She became progressively tachycardic and agitated. Antimuscarinic toxidrome was suspected and physostigmine was given with reported improvement. She was admitted to the PICU on a physostigmine infusion, requiring intermittent benzodiazepines for agitation. A urine drug screen was positive for tricyclic antidepressants (TCAs) and benzodiazepines. There was reported access to diphenhydramine in the home, but no TCAs. Eight hours after admission, the patient became acutely hypotensive with clinical seizure activity. Her cardiac rhythm devolved into a pulseless wide complex tachycardia (WCT). Notably, serial EKGs prior to the event had normal QRS intervals. Following defibrillation, her rhythm changed to PEA. Given the duration of arrest and suspected reversible etiology, the patient was cannulated to VA-ECMO. ROSC was obtained after 32 minutes of eCPR and 6 doses of sodium bicarbonate (with suspicion of sodium channel antagonism), just prior to initiation of ECMO flow. She received supportive care and was decannulated two days later. Following transfer from the PICU, an extended mass spectrometric urine panel detected lamotrigine at concentration >1 mg/L. At time of discharge to inpatient psychiatry, the patient had returned to her baseline neurologic and cardiac function. Discussion: WCT is a rare manifestation of lamotrigine toxicity associated with concentrations >25 mg/L. Clinicians should be aware of the toxicity of sodium channel antagonism, delayed onset of symptoms as seen in this case, as well as pitfalls of urine drug screening. This case is the first report of cardiac arrest from lamotrigine toxicity without coingestants in a pediatric patient.